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p48v-myb介导的转化不需要env编码的残基。

env-encoded residues are not required for transformation by p48v-myb.

作者信息

Lipsick J S, Ibanez C E

出版信息

J Virol. 1987 Mar;61(3):933-6. doi: 10.1128/JVI.61.3.933-936.1987.

DOI:10.1128/JVI.61.3.933-936.1987
PMID:3027417
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC254042/
Abstract

The v-myb oncogene of avian myeloblastosis virus induces acute myeloblastic leukemia in chickens and transforms avian myeloid cells in vitro. The protein product of this oncogene, p48v-myb, is partially encoded by the retroviral gag and env genes. We demonstrated that the env-encoded carboxyl terminus of p48v-myb is not required for transformation. Our results showed, in addition, that a coding region of c-myb which is not essential for transformation was transduced by avian myeloblastosis virus.

摘要

禽成髓细胞瘤病毒的v-myb癌基因可在鸡中诱发急性髓细胞白血病,并在体外转化禽髓细胞。该癌基因的蛋白质产物p48v-myb部分由逆转录病毒的gag和env基因编码。我们证明p48v-myb的env编码羧基末端对于转化并非必需。此外,我们的结果表明,禽成髓细胞瘤病毒转导了c-myb的一个对转化并非必需的编码区域。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/97a5e3c3f512/jvirol00094-0306-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/193d2a87b99e/jvirol00094-0304-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/a16d1d4bf315/jvirol00094-0305-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/219324d3f434/jvirol00094-0305-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/97a5e3c3f512/jvirol00094-0306-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/193d2a87b99e/jvirol00094-0304-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/a16d1d4bf315/jvirol00094-0305-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/219324d3f434/jvirol00094-0305-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde6/254042/97a5e3c3f512/jvirol00094-0306-a.jpg

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1
env-encoded residues are not required for transformation by p48v-myb.p48v-myb介导的转化不需要env编码的残基。
J Virol. 1987 Mar;61(3):933-6. doi: 10.1128/JVI.61.3.933-936.1987.
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DNA-binding activity associated with the v-myb oncogene product is not sufficient for transformation.与v-myb癌基因产物相关的DNA结合活性不足以引发转化。
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引用本文的文献

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2
Cells transformed by a v-Myb-estrogen receptor fusion differentiate into multinucleated giant cells.由v-Myb-雌激素受体融合体转化的细胞分化为多核巨细胞。
J Virol. 1997 May;71(5):3760-6. doi: 10.1128/JVI.71.5.3760-3766.1997.
3
Oncogenic truncation of the first repeat of c-Myb decreases DNA binding in vitro and in vivo.c-Myb首个重复序列的致癌性截短在体外和体内均会降低DNA结合能力。

本文引用的文献

1
Morphological conversion of cell cultures by avian myeloblastosis virus.禽成髓细胞瘤病毒对细胞培养物的形态学转化
Virology. 1961 Oct;15:185-99. doi: 10.1016/0042-6822(61)90234-3.
2
Target cells for avian myeloblastosis virus in embryonic yolk sac and relationship of cell differentiation to cell transformation.胚胎卵黄囊中禽成髓细胞瘤病毒的靶细胞以及细胞分化与细胞转化的关系。
J Virol. 1984 Mar;49(3):841-7. doi: 10.1128/JVI.49.3.841-847.1984.
3
A putative second cell-derived oncogene of the avian leukaemia retrovirus E26.禽白血病逆转录病毒E26一种假定的第二种细胞衍生癌基因。
Mol Cell Biol. 1993 Dec;13(12):7334-48. doi: 10.1128/mcb.13.12.7334-7348.1993.
4
Individual repeats of Drosophila Myb can function in transformation by v-Myb.果蝇Myb的各个重复序列可通过v-Myb发挥转化功能。
J Virol. 1993 Dec;67(12):7332-9. doi: 10.1128/JVI.67.12.7332-7339.1993.
5
The carboxyterminus of human c-myb protein stimulates activated transcription in trans.人类c-myb蛋白的羧基末端可反式刺激激活转录。
Nucleic Acids Res. 1994 Jul 11;22(13):2466-75. doi: 10.1093/nar/22.13.2466.
6
Mutations in the DNA-binding and transcriptional activation domains of v-Myb cooperate in transformation.v-Myb的DNA结合域和转录激活域中的突变在转化过程中协同作用。
J Virol. 1995 Apr;69(4):2515-24. doi: 10.1128/JVI.69.4.2515-2524.1995.
7
v-myb does not prevent the expression of c-myb in avian erythroblasts.v-myb并不阻止c-myb在禽类成红细胞中的表达。
J Virol. 1987 Oct;61(10):3284-7. doi: 10.1128/JVI.61.10.3284-3287.1987.
8
DNA-binding activity associated with the v-myb oncogene product is not sufficient for transformation.与v-myb癌基因产物相关的DNA结合活性不足以引发转化。
J Virol. 1988 Nov;62(11):4398-402. doi: 10.1128/JVI.62.11.4398-4402.1988.
9
Structural and functional domains of the myb oncogene: requirements for nuclear transport, myeloid transformation, and colony formation.myb癌基因的结构和功能结构域:核转运、髓系转化和集落形成的要求。
J Virol. 1988 Jun;62(6):1981-8. doi: 10.1128/JVI.62.6.1981-1988.1988.
10
Specific amino acid substitutions are not required for transformation by v-myb of avian myeloblastosis virus.禽成髓细胞瘤病毒的v-myb基因进行转化并不需要特定的氨基酸替换。
J Virol. 1988 Mar;62(3):1093-6. doi: 10.1128/JVI.62.3.1093-1096.1988.
Nature. 1983;306(5941):395-7. doi: 10.1038/306395a0.
4
Tripartite structure of the avian erythroblastosis virus E26 transforming gene.禽成红细胞增多症病毒E26转化基因的三方结构。
Nature. 1983;306(5941):391-5. doi: 10.1038/306391a0.
5
The product of the retroviral transforming gene v-myb is a truncated version of the protein encoded by the cellular oncogene c-myb.逆转录病毒转化基因v-myb的产物是细胞癌基因c-myb编码的蛋白质的截短版本。
Cell. 1983 Jun;33(2):345-55. doi: 10.1016/0092-8674(83)90416-6.
6
Identification of the leukemogenic protein of avian myeloblastosis virus and of its normal cellular homologue.禽成髓细胞瘤病毒致白血病蛋白及其正常细胞同源物的鉴定。
Proc Natl Acad Sci U S A. 1983 May;80(10):2834-8. doi: 10.1073/pnas.80.10.2834.
7
Nucleotide sequence of the retroviral leukemia gene v-myb and its cellular progenitor c-myb: the architecture of a transduced oncogene.逆转录病毒白血病基因v-myb及其细胞起源基因c-myb的核苷酸序列:一种转导癌基因的结构
Cell. 1982 Dec;31(2 Pt 1):453-63. doi: 10.1016/0092-8674(82)90138-6.
8
Nucleotide sequence of the transforming gene of avian myeloblastosis virus.禽成髓细胞瘤病毒转化基因的核苷酸序列。
Science. 1982 Jun 25;216(4553):1421-3. doi: 10.1126/science.6283631.
9
Replicating, differentiated macrophages can serve as in vitro targets for transformation by avian myeloblastosis virus.正在复制的、分化的巨噬细胞可作为禽成髓细胞瘤病毒体外转化的靶细胞。
J Virol. 1981 Jan;37(1):488-92. doi: 10.1128/JVI.37.1.488-492.1981.
10
The genome and the intracellular RNAs of avian myeloblastosis virus.禽成髓细胞瘤病毒的基因组与细胞内RNA
Cell. 1981 Jan;23(1):279-90. doi: 10.1016/0092-8674(81)90292-0.